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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Protein kinase C (PKC) inhibitors inhibit primary (1-0) but not secondary (1-1) or cloned cytotoxic T lymphocytes.

The isoquinolinesulfonamide PKC inhibitors H-7 and H-8 inhibit primary, in vivo generated cytotoxic T lymphocyte (CTL) activity by 50% at concentrations approximating their reported Ki values for PKC, 6 uM and 15 uM respectively. However, a greater than ten-fold higher concentration of H-7 (100 uM) is required to reduce secondary or clone 8F CTL-mediated cytotoxicity by 50%. At this concentration H-7 is also reported to inhibit calmodulin (CaM)-dependent enzymes. To distinguish between the effect of 100 uM H-7 on PKC versus CaM the napthalenesulfonamide CaM antagonist W-7 was investigated. W-7 inhibited primary, secondary and clone 8F CTL-mediated cytolysis by 50% near its reported Ki value for CaM-dependent kinase activity, 12 uM. We conclude that W-7 and 100 uM H-7 reduce cytolysis by inhibiting CaM-dependent reactions and not PKC. Thus, these findings indicate that primary killers require both PKC- and CaM-dependent activation pathways for lethal hit delivery, whereas highly lytic cultured CTL use only one pathway dependent upon CaM.[1]


  1. Protein kinase C (PKC) inhibitors inhibit primary (1-0) but not secondary (1-1) or cloned cytotoxic T lymphocytes. Howcroft, T.K., Tatum, S.M., Cosgrove, J.M., Lindquist, R.R. Biochem. Biophys. Res. Commun. (1988) [Pubmed]
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